Gout, with a section on ocular disease in the gouty

by Llewellyn J. Llewellyn

Gastro-Intestinal Disorders.—It is a matter of common experience that acute attacks of gout are often preceded by or associated with flatulence, heartburn, acidity, loss of appetite, confined bowels, scanty, high-coloured urine, and a feeling of lassitude. In short, nothing is more certain than that exacerbations or relapses very commonly follow symptoms referable to gastro-intestinal and hepatic disorders.

How well established is it that these subjects after unusual, though not necessarily excessive, indulgence at the table, almost inevitably, and sometimes almost immediately, suffer twinges in the big toe, if not frank outbreaks of gout. Such reaction seems to indicate clearly that the functional disturbances in the alimentary tract stand in some causal relation to the subsequent arthritic phenomena. The assumption gains colour, too, from the very certainty with which freedom from such gouty manifestations is attained by abstinence from, or more moderate indulgence in, articles of diet predisposing to such ebullitions.

So much by way of prelude as to the probability—attested by clinical observation and the results of treatment—that the intestinal canal is often the source of the responsible microbe or toxin. Let us now pass to consider what factors other than an oral sepsis may favour the incidence of functional disorders of the alimentary tract.

Variations in Free HCL.—Some years ago Grübe and Falkenstein found that in gout the hydrochloric acid of the gastric juice, far from being increased, was in most cases diminished or wholly wanting.

Now, as we know, the gastric juice when of normal acidity is quite capable of dealing with moderate quantities of pathogenic bacteria. But in the presence of oral sepsis it is probable that a greater number are swallowed than can be satisfactorily coped with.

Given therefore excess of pathogenic organisms and relative insufficiency of free HCL, conditions favourable to the growth of bacteria ensue, while incidentally the chance of such reaching the intestine is materially enhanced.

When, however, the defensive barrier is wholly withdrawn, viz. when there is an absence of free HCL, then of course the necessary inhibition of microbic growth fails of achievement. Moreover, also owing to diminished acidity, ill-digested protein substances gain access to the intestine, and their subsequent putrefaction is favoured.

In opposition to the foregoing, many hold that an excess of free HCL in gout is not uncommon, and unquestionably some are thus troubled. The pernicious effects of the hyperchlorhydria are accentuated by the fact that intestinal indigestion ensues secondarily, owing to the acid chyme completely antagonising pancreatic secretion and thus impairing digestive capacity.

Intestinal rather than gastric indigestion is, I think, more typical of the gouty subject. It will be recalled that the food nucleins are unaffected by the gastric juice, and though the protein moiety is split off from the nucleinic acid by the pancreatic ferments, yet neither the poly- nor the mono-nucleotides are thereby acted upon. It is in truth the succus entericus with its nucleotidase that plays the most important digestive rôle as regards nucleins, breaking them up into nucleosides which are, to a large extent, absorbed as such.